The overexpression of CARL suppressed mitochondrial fission, apoptosis and ischaemia/reperfusion (I/R) injury by directly inhibiting the expression of miR‐539 and subsequently up‐regulating the level of its target prohibitin 2 (PHB2).29 The modulation of CARL‐miR‐539–PHB2 expression might provide a novel approach for the treatment of ischaemic heart disease (IHD). The gene discussed is PHB2; the disease is heart disorder.